A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation
Atherosclerotic plaques are fatty deposits that form in the walls of major arteries and are one of the major causes of heart attacks and strokes. Macrophages are the main immune cells in plaques and macrophage dynamics influence whether plaques grow or regress. Macrophage proliferation is a key proc...
| Autors principals: | , , |
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| Format: | Journal article |
| Idioma: | English |
| Publicat: |
Springer
2024
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| _version_ | 1826313367043702784 |
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| author | Chambers, KL Watson, MG Myerscough, MR |
| author_facet | Chambers, KL Watson, MG Myerscough, MR |
| author_sort | Chambers, KL |
| collection | OXFORD |
| description | Atherosclerotic plaques are fatty deposits that form in the walls of major arteries and are one of the major causes of heart attacks and strokes. Macrophages are the main immune cells in plaques and macrophage dynamics influence whether plaques grow or regress. Macrophage proliferation is a key process in atherosclerosis, particularly in the development of mid-stage plaques, but very few mathematical models include proliferation. In this paper we reframe the lipid-structured model of Ford et al. (J Theor Biol 479:48–63, 2019. https://doi.org/10.1016/j.jtbi.2019.07.003) to account for macrophage proliferation. Proliferation is modelled as a non-local decrease in the lipid structural variable. Steady state analysis indicates that proliferation assists in reducing eventual necrotic core lipid content and spreads the lipid load of the macrophage population amongst the cells. The contribution of plaque macrophages from proliferation relative to recruitment from the bloodstream is also examined. The model suggests that a more proliferative plaque differs from an equivalent (defined as having the same lipid content and cell numbers) recruitment-dominant plaque in the way lipid is distributed amongst the macrophages. The macrophage lipid distribution of an equivalent proliferation-dominant plaque is less skewed and exhibits a local maximum near the endogenous lipid content. |
| first_indexed | 2024-09-25T04:13:43Z |
| format | Journal article |
| id | oxford-uuid:4f829a63-b71b-41f7-af17-a64e2ba8ca39 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-09-25T04:13:43Z |
| publishDate | 2024 |
| publisher | Springer |
| record_format | dspace |
| spelling | oxford-uuid:4f829a63-b71b-41f7-af17-a64e2ba8ca392024-07-09T20:07:55ZA Lipid-Structured Model of Atherosclerosis with Macrophage ProliferationJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4f829a63-b71b-41f7-af17-a64e2ba8ca39EnglishJisc Publications RouterSpringer2024Chambers, KLWatson, MGMyerscough, MRAtherosclerotic plaques are fatty deposits that form in the walls of major arteries and are one of the major causes of heart attacks and strokes. Macrophages are the main immune cells in plaques and macrophage dynamics influence whether plaques grow or regress. Macrophage proliferation is a key process in atherosclerosis, particularly in the development of mid-stage plaques, but very few mathematical models include proliferation. In this paper we reframe the lipid-structured model of Ford et al. (J Theor Biol 479:48–63, 2019. https://doi.org/10.1016/j.jtbi.2019.07.003) to account for macrophage proliferation. Proliferation is modelled as a non-local decrease in the lipid structural variable. Steady state analysis indicates that proliferation assists in reducing eventual necrotic core lipid content and spreads the lipid load of the macrophage population amongst the cells. The contribution of plaque macrophages from proliferation relative to recruitment from the bloodstream is also examined. The model suggests that a more proliferative plaque differs from an equivalent (defined as having the same lipid content and cell numbers) recruitment-dominant plaque in the way lipid is distributed amongst the macrophages. The macrophage lipid distribution of an equivalent proliferation-dominant plaque is less skewed and exhibits a local maximum near the endogenous lipid content. |
| spellingShingle | Chambers, KL Watson, MG Myerscough, MR A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title | A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title_full | A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title_fullStr | A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title_full_unstemmed | A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title_short | A Lipid-Structured Model of Atherosclerosis with Macrophage Proliferation |
| title_sort | lipid structured model of atherosclerosis with macrophage proliferation |
| work_keys_str_mv | AT chamberskl alipidstructuredmodelofatherosclerosiswithmacrophageproliferation AT watsonmg alipidstructuredmodelofatherosclerosiswithmacrophageproliferation AT myerscoughmr alipidstructuredmodelofatherosclerosiswithmacrophageproliferation AT chamberskl lipidstructuredmodelofatherosclerosiswithmacrophageproliferation AT watsonmg lipidstructuredmodelofatherosclerosiswithmacrophageproliferation AT myerscoughmr lipidstructuredmodelofatherosclerosiswithmacrophageproliferation |